Digestive manifestations due to uremia and uremic toxins are multiple in patients with chronic kidney disease (CKD) on hemodialysis (HD). As much as 79 percent of these patients report gastrointestinal symptoms manifested as nausea, vomiting, dry mouth, dysgeusia, halitosis, pyrosis, abdominal pain, bloating, diarrhea (1,2). Due to many pathogenic mechanisms, the prevalence of gastro-duodenal peptic ulcer disease is higher in HD subjects than in general population, but comparable in frequency with nondialyzed CKD patients (3-5). A recent published 10 years-study presented that the incidence of peptic ulcer disease is 4 times higher in patients with CKD and 9.4 times higher in individuals on chronic HD compared to the general population (6). Regarding localization, gastric ulcers are twice more frequent documented than duodenal ulcers (6-8). An imbalance between protective and aggressive mucosal factors in favor of the last ones is noticed in HD patients. Chronic dialysis stress, intradialysis hypotension (causing mucosal hypo-perfusion), anemia, intra-dialysis anticoagulant, metabolic acidosis, potentially ulcerogenic medication (steroids, non-steroid anti-inflammatory and antiplatelet drugs) lead to high frequencies of peptic ulcer disease (9). Since the appearance of ulcerous lesions, the risk of their complications (e.g.: hemorrhages, perforations, penetrating injuries) is much higher than in general population. One recent cohort study in Taiwan showed that the incidence of gastro-duodenal bleedings is double in CKD patients and 5 times higher in HD ones (2). Subsequently, common comorbidities such as diabetes, liver cirrhosis and ischemic heart disease participate as pathogens in digestive bleedings (10).
An adequate diagnosis and monitoring of peptic ulcer disease in dialysis patients represent a constant concern of our clinical practice, because of the high prevalence of this kind of pathology, the life-threatening potential complications and the complexity of the treatment. Therefore, further on we discuss the case of an atypical peptic ulcer disease in a chronic HD patient.

Patients with chronic renal disease frequently display eso-gastro-duodenal associated pathology: anorexia, heartburn, nausea, vomiting, abdominal pain, gastric motility disorder so far as gastroparesis
some of these symptoms decline once the substitution therapy of the renal function is initiated through hemodialysis, and some persist because of the interdialytic metabolic acidosis, used anticoagulant in dialysis or complementary therapies.
The most severe clinical manifestation is superior digestive hemorrhage, with multiple intricate causes (mucosal lesions induced by gastrin, angiodysplasia including GAVE - gastric antral vascular ectasia, treatments with lesion potential - NSAIDs, corticoids, oral iron drugs, mucosa inflammation under uremic toxins or oxygen radicals, gastric and intestinal wall edema due to interdialytic hypervolemia, malnutrition). The gastric hyperacidity induced injuries in renal patients are often esophagitis, gastritis, duodenitis and gastro-duodenal ulcer.